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Cho, Charles Young,1974-
Role of oxidative stress in two models of insulin resistance within primary rat adipocytes.
M. Sc. -- University of Toronto, 1999
Ottawa :National Library of Canada = Bibliothèque nationale du Canada,[2000]
2 microfiches
Includes bibliographical references.
Insulin's major action is to increase the flux of glucose into insulin sensitive tissues. A decreased biological response to insulin, termed insulin resistance, is induced in adipocytes by chronic incubation in high glucose and insulin (high G/I), or glucosamine, or hydrogen peroxide. The hypothesis that resistance to insulin stimulated glucose uptake caused by high G/I and glucosamine is due to enhanced production of reactive oxygen species or oxidative stress was tested. Isolated rat adipocytes incubated in high G/I or glucosamine showed insulin resistance while the antioxidant and glutathione (GSH) precursor N-acetylcysteine (NAC) and GSH monoethyl ester prevented resistance. However, the antioxidant [alpha]-tocopherol and ebselen had no significant effect. Similarly the MAPKK (MEK) inhibitor, PD98059, and the p38 MAPK inhibitor, SB203580, could not prevent insulin resistance. Intracellular GSH was decreased by glucosamine, and increased by high G/I. NAC prevented the decreased levels of GSH caused by glucosamine. The data support a role for GSH in the pathogenesis of insulin resistance but the role of oxidative stress is not clear.